title: Effects of ARHI on breast cancer cell biological behavior regulated by microRNA-221.
abstract: The aplysia ras homolog member I (ARHI) is a tumor suppressor gene and is downregulated in various cancers. The downregulation of ARHI was regulated by miR-221 in prostate cancer cell lines. However, it has not been reported whether ARHI is regulated by miR-221 in breast cancer. Here, we reported that the ARHI protein level was downregulated in breast cancer tissues and breast cancer cell lines. The overexpression of ARHI could inhibit cell proliferation and invasion and induce cell apoptosis. To address whether ARHI is regulated by miR-221 in breast cancer cell lines, the results in this study showed that a significant inverse correlation existed between ARHI and miR-221. MiR-221 displayed an upregulation in breast cancer tissues and breast cancer cell lines. The inhibition of miR-221 induced a significant upregulation of ARHI in MCF-7 cells. To prove a direct interaction between miR-221 and ARHI mRNA, ARHI 3'UTR, which includes the potential target site for miR-221, was cloned downstream of the luciferase reporter gene of the pMIR-REPORT vector to generate the pMIR-ARHI-3'UTR vector. The results confirmed a direct interaction of miR-221 with a target site on the 3'UTR of ARHI. In conclusion, ARHI is a tumor suppressor gene that is downregulated in breast cancer. The overexpression of ARHI could inhibit breast cancer cell proliferation and invasion and induce cell apoptosis. This study demonstrated for the first time that the downregulation of ARHI in breast cancer cells could be regulated by miR-221.
authors.affiliation: Department of Oncology, Chinese PLA General Hospital, No. 28, FuXing Road, Beijing, 100853, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Li
authors.forename: Mei
authors.initials: M
authors.lastname: Liu
authors.forename: Yanjun
authors.initials: Y
authors.lastname: Zhang
authors.forename: Chun
authors.initials: C
authors.lastname: Han
authors.forename: Junhao
authors.initials: J
authors.lastname: You
authors.forename: Junlan
authors.initials: J
authors.lastname: Yang
authors.forename: Cheng
authors.initials: C
authors.lastname: Cao
authors.forename: Shunchang
authors.initials: S
authors.lastname: Jiao
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D017209:Apoptosis / Q000235:genetics; D001483:Base Sequence; D015153:Blotting, Western; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002453:Cell Cycle / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D002470:Cell Survival / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008156:Luciferases / Q000235:genetics / Q000378:metabolism; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000235:genetics*; D009154:Mutation; D016376:Oligonucleotides, Antisense / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020741:rho GTP-Binding Proteins / Q000235:genetics* / Q000378:metabolism
chemical_list: D020413:3' Untranslated Regions; D008156:Luciferases; D035683:MicroRNAs; D016376:Oligonucleotides, Antisense; D020741:rho GTP-Binding Proteins; C117386:DIRAS3 protein, human; C525709:MIR221, human